Approximately 20% of cardiac output is delivered primarily to the brain by two carotid arteries and two vertebral arteries. The blood is pumped by the heart at a mean systolic pressure of around 7.2 PSI and moves through a network of, progressively decreasing in caliber, elastic muscular conduits (arteries), ending in biologically active membranes (capillaries). Approximately 1% of the population has a weakening in the muscular layer at the branching point of certain cerebral arteries. The intraluminal pressure can expand the artery into an outpouching called an aneurysm at the site of the weakening. Furthermore, the pressure can become unduly elevated or a degenerative disease can attack and weaken the wall further. Under these conditions the aneurysms can rupture or tear.
Most of the weakened arteries are on the surface of the brain and directly in contact with the cerebrospinal fluid. The aneurysm rupture has a spectrum of presentations related to the opening of the high pressure arterial system (around 7 PSI) into the low pressure cerebrospinal fluid system (around 0.3 to 1.2 PSI). Although many times only a small amount of blood will leak into the cerebrospinal fluid and the arterial opening will close by clot formation, a huge 2 to 4 mm rent in the aneurysm can occur. This will allow a high pressure direct spout of blood, saturating the cerebrospinal fluid and/or eroding an opening into the adjacent brain, before the leak is sealed by clot formation. Mortality rate for this congenital disease is quite high. Thirty-four to forty percent die during the initial bleeding. Another 30-40% of the survivors die within the following four weeks. Thus, approximately 60% of individuals who develop a ruptured aneurysm die. Autopsy and incidence studies indicate that about 1% of the population have aneurysms. Currently, medical care is directed toward increasing the chance of survival after the aneurysm has ruptured and the individual reaches the hospital.
When blood enters the cerebrospinal fluid, vasospasm can occur and the arteries in contact with the cerebrospinal fluid decrease in calibre, resulting in decreased blood volume delivery to the capillary membrane and metabolizing tissue. The consequent decreased oxygen tension causes ischemia. Severe ischemia can cause cell death or necrosis and a permanent neurological function loss. The exact mechanism for initiation of vasospasm is unknown, but it is thought to involve blood borne factors which are liberated into the cerebrospinal fluid. The materials causing the vasospasm have not been identified though they have been found in blood and cerebrospinal fluid of subarachnoid hemorrhage. There is a positive correlation between the amount of subarachnoid blood and cerebral vasospasm observed.
After an initial subarachnoid hemorrhage, vasospasm seems to occur during the following time course: no spasm for the first through the fourth days, vasospasm after 5 to 22 days. A repeated subarachnoid hemorrhage, however, shortens the initial non-spasm period.
Currently the physician must balance the risks of treating a patient having subarachnoid bleeding. Although the optimal time to operate is between 7-14 days, vasospasm is likely to occur after only 4 days. Thus, by delaying surgery until 7-14 days after the initial bleed the surgical results improve and technically the surgery is easier, but more patients will die from vasospasm or repeat bleed.
Most attempts, to date, to treat or prevent intracranial arterial spasm have not been successful. The best predictor of vasospasm is the amount of blood within the basal subarachnoid cisterns four days after a spontaneous subarachnoid hemorrhage. This can be visualized directly or by a CT scan. The apparatus for cerebrospinal fluid exchange described in the present invention provides prophylaxis against symptomatic intra-cranial arterial spasm by removing blood and blood byproducts from the cerebrospinal fluid and by cooling the circulating cerebrospinal fluid to improve injured brain survival. Furthermore, the apparatus monitors normal cerebrospinal fluid pH, temperature, pressure and percent transmittance, providing immediate evidence of a repeat subarachnoid hemorrhage. This procedure will be much safer than current procedures which involve the removal of clotted blood and vasospastic effects from the subarachnoid cisterns. This has included mechanical removal by the surgeon of blood clots in the area of surgical exposure, drainage of the subarachnoid spaces, and ventricular cisternal irrigation for 7-14 days.